Voluntary alcohol drinking & caloric intake in rats exposed to crowding stress

Voluntary alcohol drinking & caloric intake in rats exposed to crowding stress

Nagaraja, H S

Background & objectives: Alcohol intake in animals is regulated in much the same way as intake of food. The effect of alcohol on feeding behaviour is not well documented. The objective of this study was to test whether alcohol was ingested as a source of calories after crowding stress in rats.

Methods: Male albino rats were exposed to crowding stress continuously for two weeks and the effect of stress on the body weight, food intake, voluntary alcohol consumption and caloric intake in terms of food and alcohol was studied.

Results: A significant decrease in the body weight was seen after one (P

Interpretation & conclusion: Crowding stress decreased the body weight gain throughout the period of stress. Chronic stress for two weeks increased the voluntary alcohol consumption and total caloric intake. Food intake alone seemed insufficient to provide the extra demand of energy due to prolonged stress and hence, the rats may be drinking increasing amounts of alcohol (when provided) to supply the extra energy required to combat stress.

Key words Alcohol – caloric intake – crowding – food intake

There is a growing interest in the possibility that stress affects health not only through direct psychophysiological processes, but also by modifying behaviours that affect such as physical exercise, smoking and food choices. Chronic stress itself causes disturbances of the circadian rhythm in animals1,2 and has also been reported to cause behavioural and physiological abnormalities such as decreased food intake, change in certain types of behaviour, hypothermia and an elevation in plasma glucocorticoid levels3,4. Although the mechanism mediating the chronic stress influences is far from being understood; it is generally accepted that the neuroendocrine systems such as the hypothalamicpituitary-adrenal (HPA) axis and the sympathetic nervous system play an important role in transforming psychological influences into functional changes in behaviour and biology.

The effects of alcohol on the stress response are complex. The most extensively studied properties of ethanol that pertain to its level of ingestion include its psychoactive effects and energy values5. Alcohol consumption can reduce the magnitude of an organism’s response to stress6. The most frequently used approach for determining the stress response dampening effects of alcohol involves monitoring various physiological responses7. Numerous studies have found that stress increases alcohol consumption in animals and that individual animals may differ in the amount of alcohol they consume in response to stress8-10. In rodents alcohol intake was regulated in much the same way as food11. Alcohol was considered as a caloric substance and the appetite for alcohol was considered much the same way as the appetite for any other food12.

The effect of ethanol on the feeding behaviour of animals is scantly documented and the understanding of the factors influencing alcohol ingestion is limited. While the adverse consequences of alcohol abuse are well established, recent evidence that moderate consumption may provide protection against heart disease has prompted increased interest in the positive and negative roles of ethanol in the diet13. The aim of the present study was to test whether alcohol is ingested as a source of calorie after crowding stress in albino rats.

Material & Methods

Male Wistar rats at 12 wk of age, reared in the laboratory of Department of Physiology were used for this study. The animals weighing 200 -300g at the start of the experiment were housed in groups of two per cage for two weeks to adapt to the laboratory conditions. Before the start of the experiments, the animals had not had any experience in the intake of any other liquids besides tap water. All animals were housed under standard laboratory conditions with 12 h light: dark cycle and controlled room temperature at 29 deg C. Food pellets (Hindustan Lever Ltd. Mumbai) were available ad libitum during the study. Animals were handled daily for one week prior to experiments to minimize the nonspecific stress on the days of the experiment.

Control group: Consisted of six male rats kept under standard laboratory conditions without any stress exposure. These animals were kept in polypropylene cages (45x30X16 cm), two rats per cage.

Stressed group: Six male rats were kept in a single polypropylene cage (25x20x15 cm) in such a way that only minimum mobility was possible inside the cage. The rats were kept in this overcrowded condition continuously except on days two and eight when they were shifted to individual cages for recording the intake of food, water and alcohol.

Rats in both groups were exposed to a two-bottle choice between tap water and a 2 per cent (w/v) ethanol solution. The alcohol solution was prepared by mixing 95 per cent ethanol with water. The bottle positions were altered regularly at random to prevent place preference.

Twenty four hours food, water and voluntary alcohol intakes were recorded/after moving the rats to individual cages at the end of one, 7 and 14 days both in stressed and control groups. Total body weight, water intake, food intake and voluntary alcohol consumption were also monitored daily between 0900-1100 h in both these groups. Whole body weight was expressed as body weight changes in grams from the initial body weight, before the start of the experiment. Fluid intake (both alcohol and water) was measured recording the remaining fluid content in the bottle; 24 h food consumption was measured by weighing what was left behind in the cage, of the food provided on the previous day. The intake of 2 per cent ethanol for individual rat was transformed into the intake of absolute alcohol relative to each rat’s body weight. Caloric intake by each animal in terms of food and alcohol were calculated after taking the food intake and alcohol intake for 24 h period. All the experimental procedures were in accordance with the ethical guidelines on animal experiments and were approved by the institutional ethics committee.

Statistical analysis: Data collected were computed for mean values +/- SE. Comparison between the control and stressed groups was done by Mann-Whitney test. Analysis of changes in a parameter between days one, 7 and 14 was done by Friedman’s test.

Results

There was a significant decrease in the whole body weight after one (P

Water intake decreased significantly (P

Total caloric intake in stressed rats was significantly decreased (P

Discussion

Differences in the population density lead to endocrine responses in the individual14. Crowding was found to decrease body weight and increase adrenal epinephrine secretion, indicating that crowding may be considered as a stressful stimulus15. In the present study there was a reduction in the body weight throughout the 14 days stress period. Food intake decreased only in the initial period of stress exposure. Corticotrophin releasing hormone (CRH) is known to suppress food intake in rats16. The increased level of glucocorticoids during chronic stress in animals could suppress CRH secretion from the hypothalamus, which explains the recovery in food intake after prolonged stress17. Stress might have increased the protein catabolism and hampered the utilization of whatever food was consumed by the rats thereby causing decreased body weight after chronic stress.

When the animals were exposed to chronic stress there was a significant increase in the voluntary alcohol intake. Stressful stimuli potentially activate the HPA axis18. Thus the situation of chronic crowding might have caused adrenal corticosterone hypersecretion, which might have contributed to the enhanced ethanol consumption. Adreno corticotropic hormone (ACTH) is known to play a crucial role in the stress induced initiation of ethanol consumption behaviour in rats17,19. The observed decrease in water intake is contradictory to results of certain other studies where there was increased water intake after stress in rats20,21. The decrease in water intake after chronic stress could be due to increased ethanol intake in these rats.

Ethanol can replace fat and carbohydrates as a source of calories in the diet22. Alcohol drinking rats can immediately adjust their caloric intake over a 24 h circadian cycle. In the present study, prolonged stress made the animals recover in terms of caloric intake after one week. This is probably due to adaptation to the stress. Animals consumed more food than alcohol to combat stress up to a period of one week. In the stressed rats there is an increased energy requirement due to increased secretion of catecholamines and glucocorticoids and also due to increased locomotor activity necessitated by overcrowding. After two weeks, food intake alone seemed insufficient to supply the extra demand of energy due to stress and hence the rats drank increasing amounts of alcohol which was available ad lib along with food. Caloric intake values indicate very low energy density in food and this also might have caused increased alcohol consumption in the stressed animals.

It has been reported that rats drinking alcohol exhibit reduced food intake almost in direct proportion to the calories obtained from alcohol23. In the present study the animals showed a decrease in body weight and decreased water intake when the stress period was prolonged for two weeks confirming the earlier reports12, 22-24. There was an increase in total caloric intake after 14 days and on a chronic basis one would expect to observe a body weight gain. Yet, it did not occur. It is concluded that crowding stress decreased the body weight gain throughout the duration of stress. Chronic stress for two weeks increased the alcohol consumption and the total caloric intake, thereby supplying the extra energy required to combat the effects of stress on the body.

Acknowledgment

The authors acknowledge Ms Asha Kamath, Lecturer, Department of Community Medicine, K.M.C. Mangalore, for assistance in the statistical analysis.

References

References

1. Anderson SM, Kant GJ, De Souza EB. Effects of chronic stress on anterior pituitary and brain corticotropin releasing factor receptors. Pharmacol Biochem Behav 1993; 44 : 755-61.

2. Marti 0, Gavalda A, John T, Armario A. Effect of regularity of exposure to chronic immobilization stress on the

circadian pattern of pituitary adrenal hormones, growth hormone, and thyroid stimulating hormone in the adult male rat. Psychoneuroendocrinology 1993; 18 : 67-77.

3. Ottenweller JE, Natelson BH, Pitman DL, Drastal SD. Adrenocortical and behavioural responses to repeated stressors: toward an animal model of chronic stress and stress-related mental illness. Biol Psychiatry 1989; 26 : 829-41.

4. Restrepo C, Armario A. Chronic stress alters pituitaryadrenal function in prepubertal male rats. Psychoneuroendocrinology 1987; 12 : 393-8.

5. Heyman GM, Oldfather C. Elasticity of preference for ethanol in rats: an analysis of the reinforcing properties of ethanol. Psychol Sci 1992; 3 : 122-30.

6. Levenson RW, Sher KJ, Grossman LM, Newman J, Newlin DB. Alcohol and stress response dampening: pharmacological effects, expectancy, and tension reduction. J Abnorm Psychol 1980; 89 : 528-38.

7. Sayette MA. Does drinking reduce stress? Alcohol Res Health 1999; 23 : 250-5.

8. Gauvin DV, Moore KR, Holloway FA. Do rat strain differences in ethanol consumption reflect differences in ethanol sensitivity or the preparedness to learn? Alcohol 1993; 10 : 37-43.

9. Hilakivi – Clarke L, Lister RG. Social status and voluntary alcohol consumption in mice: interaction with stress. Psychopharmacology (Berl) 1992; 108 : 276-82.

10. Hannon R, Donlon – Bantz K. Effects of crowding on alcohol consumption by rats. J Stud Alcohol 1975; 36 1273-6.

11. Richter CP. Alcohol as a food. Q J-Stud Alcohol 1941; I : 650-62.

12. Rodgers DA, McClearn GE, Bennett EL, Hebert M. Alcohol preference as a function of its caloric utility in mice. J Comp Physiol Psychol 1963; 56 : 666-72.

13. Wannamethee SG, Shaper AG. Type of alcoholic drink and risk of major coronary heart disease ,events and all-cause mortality. Ani J Public Health 1999;189 : 685-90.

14. Chaouloff F, Zamfir 0. Psychoneuroendocrine outcomes of short-term crowding stress. Physiol Behav 1993; 54 767-70.

15. Christian JJ, Lloyd JA, Davis DE. The role of endocrines in the self-regulation of mammalian populations. Recent Prog Horm Res 1965; 21: 501-78.

16. Levine AS, Rogers B, Kneip J, Grace M, Morley JE. Effect of centrally administered corticotrophin releasing factor (CRF) on multiple feeding paradigms. Neuropharmacology 1983; 22 : 337-9.

17. Fahlke C, Engel JA, Eriksson CJP, Hard E, Soderpalm B. Involvement of corticosterone in the modulation of ethanol consumption in the rat. Alcohol 1994; 11 : 195-202.

18. Weinstock M, Poltyrev T, Schorer – Apelbaum D, Men D, McCarty R. Effect of prenatal stress on plasma corticosterone and catecholamines in response to footshock in rats. Physiol Behav 1998; 64 439-44.

19. Fahlke C, Eriksson CJP. Effect of adrenalectomy and exposure to corticosterone on alcohol intake in alcohol– preferring and alcohol-avoiding rat lines. Alcohol Alcohol 2000, 35 : 139-44.

20. Yoshida T, Okuno T, Kawabata T, Morimoto T. Salt consumption and body fluid balance during cold exposure in rats. Physiol Behav 1994; 55 : 163-7.

21. Rodriguez de Turco EB, Droy – Lefaix MT, Bazan NG. EGb 761 inhibits stress-induced polydipsia in rats. Physiol Behav 1993; 53 : 1001-2.

22. Larue-Achagiotis C, Poussard AM, Louis Sylvestre J. Effect of interscapular brown adipose tissue denervation on body weight and feed efficiency in alcohol drinking rats. Physiol Behav 1989; 46: 195-7.

23. Strbak V, Benicky J, Macho L, Jezova D, Nikodemova M. Four-week ethanol intake decreases food intake and body weight but does not affect plasma leptin, corticosterone, and insulin levels in pubertal rats. Metabolism 1998; 47 1269-73.

24. Luz J, Griggio MA, Plapler H, De-Meo-Bancher M, Carvalho-Kosmiskas JV. Effects of ethanol on energy balance of rats and the inappropriateness of intraperitoneal injection. Alc6hol 1996; 13 : 575-80.

H. S. Nagaraja & P. S. Jeganathan

Department of Physiology, Kasturba Medical College, Mangalore, India

Received May 3, 2002

Copyright Indian Council of Medical Research Sep 2002

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